Mouse pre-microRNA Expression Construct mir-140
- Known as:
- Mouse pre-microRNA Expression Construct mir-140
- Catalog number:
- mmir-140-pa-1
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sbi systeme bioscience
- Gene target:
- Mouse pre-microRNA Expression Construct mir-140
Related genes to: Mouse pre-microRNA Expression Construct mir-140
- Gene:
- MIR140 NIH gene
- Name:
- microRNA 140
- Previous symbol:
- MIRN140
- Synonyms:
- hsa-mir-140
- Chromosome:
- 16q22.1
- Locus Type:
- RNA, micro
- Date approved:
- 2004-04-23
- Date modifiied:
- 2019-01-31
Related products to: Mouse pre-microRNA Expression Construct mir-140
Related articles to: Mouse pre-microRNA Expression Construct mir-140
- To evaluate the clinical efficacy of close-to-bone needling (CBN) in patients with knee osteoarthritis (KOA) and to explore its underlying mechanisms. - Source: PubMed
Publication date: 2026/08/15
Lu YumeiWu HuiyingFu NiniSu QianZeng QiHe YifanRen Yi - Long intergenic non-coding RNAs (lincRNAs) are key epigenetic regulators of genome function, yet their evolutionary dynamics following whole-genome duplication (WGD) events remain poorly understood. Salmonids, which underwent a lineage-specific autotetraploidization (salmonid-specific WGD, ~88-100 million years ago), provide an excellent model to investigate the retention, divergence, and functional potential of recently duplicated non-coding elements. LincRNA repertoires were compared across five genome-annotated salmonids (, , , , and ) and their closest non-duplicated relative, northern pike (). LincRNAs represented ~5-7% of annotated genes in all salmonids except (18%). Sequence conservation was low relative to coding genes, with only 11-68 highly similar (e-value < 1 × 10; similarity > 70% and alignments > 100 nucleotides) putative orthologues shared between salmonids and northern pike, and 161-338 among salmonids alone. Synteny conservation was modest in lincRNAs, with lower conservation in putative orthologues (8-16%) compared to putative ohnologues (8-33%). Secondary structure conservation was associated with sequence similarity ( = -0.45; = 2.2 × 10), and the association was stronger among WGD ohnologues than orthologues. In and , lincRNA putative ohnologues showed weaker expression correlations than coding genes, suggesting widespread regulatory divergence, possibly through neo- and subfunctionalisation. Conserved salmonid lincRNAs showed enriched predicted interactions with miRNAs involved in tumour suppression, brain, bone, and muscle development (e.g., , , , , , and ), a finding supported by limited transcriptomic data. Although salmonid WGD expanded lincRNA repertoires, lincRNAs have undergone rapid sequence and transcriptional divergence, with limited conservation across species based on sequence similarity, chromosomal position, synteny, and secondary structure. A subset of conserved lincRNAs retains structural features and regulatory signatures consistent with roles as miRNA sponges in brain, skeletal, and muscle development and tumour suppression, potentially acting within conserved regulatory networks. These findings provide new insights into lincRNA evolution following genome duplication and highlight the need for experimental validation of their regulatory functions. - Source: PubMed
Publication date: 2026/09/02
García-Pérez IsabelGarcia de la Serrana Daniel - Alzheimer's disease (AD) is responsible for 70% of dementia cases worldwide, with tau hyperphosphorylation and amyloid-β plaque accumulation representing its core pathological hallmarks. Genetic predisposition, oxidative stress, and neuroinflammation contribute to disease onset and progression. Non-coding ribonucleic acids (ncRNAs) are a class of RNAs which control gene expression and whose dysregulation in AD patients has been linked to amyloid production, neuroinflammation, and mitochondrial dysfunction, which ranges from impaired energy metabolism to disrupted mitochondrial biogenesis and dynamics. Our descriptive systematic review surveyed the involvement of ncRNAs in mitochondrial dysfunction in AD across experimental and clinical literature. We identified multiple microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) that directly regulate mitophagy, mitochondrial biogenesis, mitochondrial autophagic, and apoptotic pathways, mitochondrial dynamics, and protein import mechanisms in AD models. Among the most important candidates demonstrating clinical dysregulation, miR-140 and lncRNA NEAT1 regulate mitophagy, while miR-9, miR-34a, miR-146a, miR-155, and miR-485 are implicated in mitochondrial biogenesis and miR-204 in mitochondrial autophagy. LncRNA BDNF-AS, miR-148a-3p, miR-21-5p, and miR-103a-3p emerged as regulators of the mitochondrial apoptosis pathway with confirmed clinical dysregulation. Multiple ncRNAs control mitochondrial dynamics, of which miR-195, miR-124, and miR-455-3p have also been studied in AD patients. Additionally, several ncRNAs were found to indirectly regulate mitochondrial fission, autophagy, and apoptosis, although the underlying mechanisms require further characterization. Thus, while ncRNA-centered AD research is in its early stages, current mechanistic and translational evidence supports mitochondrially relevant ncRNAs as promising candidates for biomarker and therapeutic development. - Source: PubMed
Publication date: 2026/09/15
Mocrei-Rebrean Ștefania-MariaRăzniceanu VladPintilie Sebastian RomeoBerindan-Neagoe Ioana - Osteoarthritis (OA) is the most prevalent degenerative joint disease and a leading cause of chronic pain and disability worldwide, particularly among aging populations. It is characterized by progressive degeneration of articular cartilage, synovial inflammation, subchondral bone remodeling, and metabolic alterations in the infrapatellar fat pad, reflecting pathology across the entire joint microenvironment. The onset and progression of OA are driven by complex interactions among mechanical stress, aging, obesity, and metabolic dysregulation, which collectively disrupt joint homeostasis. Mechanical injury and cartilage damage induce the release of damage-associated molecular patterns, activating innate immune receptors on chondrocytes and synovial cells. This promotes the production of pro-inflammatory mediators, including interleukin-1β, tumor necrosis factor-α (TNF-α), interleukin-6, and interleukin-17, which contribute to extracellular matrix degradation and cartilage deterioration. MicroRNAs (miRNAs), small non-coding RNAs that regulate gene expression post-transcriptionally, have emerged as key modulators in OA pathogenesis. They regulate chondrocyte proliferation, apoptosis, extracellular matrix turnover, inflammation, and osteochondral remodeling. Notably, certain miRNAs exhibit mechanosensitive properties, responding to altered biomechanical loading and translating mechanical stimuli into gene regulatory responses. This review synthesizes current evidence on the roles of miRNAs in OA, focusing on their regulatory functions across joint tissues, including cartilage, synovium, subchondral bone, and the infrapatellar fat pad. Key miRNAs such as miR-140, miR-146a, miR-27b, miR-34a, miR-155, and mechanosensitive miR-365 are discussed, along with their interactions with major inflammatory and degenerative signaling pathways. Their potential as diagnostic biomarkers and therapeutic targets is also highlighted. - Source: PubMed
Publication date: 2026/07/21
Safiyyu Mujitapha UmarSyed Nazmul HudaAzlan MaryamZain Muhammad Rajaei Ahmad MohdNurul Asma Abdullah - MicroRNAs, small noncoding RNA molecules, are pivotal regulators of gene expression and have been increasingly implicated in the molecular mechanisms underlying addiction. In this study, we investigated microRNA expression profiles in postmortem nucleus accumbens tissue, a key brain region for reward and addiction, from individuals with 6-monoacetylmorphine confirmed heroin-associated polysubstance intoxication (6-MAM-HAPI) (n = 20) compared with non-user individuals (n = 20). Total RNA was isolated from the tissues with "RNAzol®RT," and cDNA was obtained and measured by qRT-PCR. MicroRNA expression levels were calculated by the 2 method. Our study revealed a distinct pattern of dysregulation, with downregulation of miR-132, miR-140, miR-181a, miR-206, miR-212, and miR-339-5p, alongside a significant upregulation of miR-133b in nucleus accumbens of 6-MAM-HAPI. These findings provide preliminary postmortem evidence suggesting possible miRNA expression changes in the nucleus accumbens in the context of 6-MAM-HAPI. - Source: PubMed
Publication date: 2026/07/28
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